It has long been known that iodide appears in the milk of mammals. The levels of iodide in the milk of a variety of mammals including humans are 20-30 fold higher than that present in the maternal plasma. Since about 50% of the iodide in milk is incorporated into milk proteins, the mechanisms that drive the accumulation of iodide in milk could include the functioning of an iodide transporter and/or enzymes involved in iodide incorporation into proteins. Early experiments showed a decreased .sup.131 I accumulation in milk when lactating rats were injected with perchlorate (an inhibitor of the iodide transporter) or methimazole (an inhibitor of peroxidase). Perchlorate was more potent in inhibiting total .sup.131 I uptake, whereas methimazole, primarily inhibited .sup.131 I binding to milk proteins. These in vivo studies suggest that both an iodide transporter and a peroxidase enzyme are present in mammary cells, and are involved in the accumulation of iodide in milk during lactation.
Studies in the literature focusing on the hormonal regulation of iodide transport in the mammary gland are limited. It has been reported that thyroid stimulating hormone (TSH) or thyroxin injected into lactating rats had no effect on .sup.131 I secretion into milk. In addition, prolactin (PRL), growth hormone (GH), insulin or cortisol had no effect on iodide uptake into cultured mammary tissues taken from lactating rats.
Studies in the literature concerning iodide uptake in neoplastic mammary cells reported that radioactive iodide concentration in biopsied human breast tissue with carcinoma or dysplasia is higher than in histologically normal tissues from the same patients.